Within the last few years, there have been an increased number of clinical studies involving urinary microbiota. Low-biomass microbiome sequencing (e.g., urine, lung, placenta, blood) is easily biased by contamination or cross-contamination. So far, a few critical steps, from sampling urine to processing and analyzing, have been described (e.g., urine collection modality, sample volume size, snap freezing, negative controls usage, laboratory risks for contamination assessment, contamination of negative results reporting, exploration and discussion of the impact of contamination for the final results, etc.) We performed a literature search (Pubmed, Scopus and Embase) and reviewed the published articles related to urinary microbiome, evaluating how the aforementioned critical steps to obtain unbiased, reliable results have been taken or have been reported. We identified different urinary microbiome evaluation protocols, with non-homogenous reporting systems, which can make gathering results into consistent data for similar topics difficult and further burden the already so complex emerging field of urinary microbiome. We concluded that to ease the progress in this field, a joint approach from researchers, authors and publishers would be necessary in order to create mandatory reporting systems which would allow to recognize pitfalls and avoid compromising a promising field of research.

Gallbladder disorders encompass a spectrum from congenital anomalies to inflammatory and neoplastic conditions, frequently requiring surgical intervention. Epithelial abnormalities like adenoma and metaplasia have the potential to progress to carcinoma, emphasizing the importance of histopathological assessment for early detection of malignancy. Gallbladder cancer (GBC) may be incidentally discovered during cholecystectomy for presumed benign conditions, underscoring the need for a thorough examination. However, the lack of clarity regarding the molecular mechanisms of GBC has impeded diagnostic and therapeutic advancements. Timely detection is crucial due to GBC’s aggressive nature and poor prognosis. Chronic inflammation plays a central role in carcinogenesis, causing DNA damage and oncogenic alterations due to persistent insults. Inflammatory cytokines and microRNAs are among the various mediators contributing to this process. Gallbladder calcifications, particularly stippled ones, may signal malignancy and warrant preemptive removal. Molecular pathways involving mutations in oncogenes and tumor suppressor genes drive GBC pathogenesis, with proposed sequences such as gallstone-induced inflammation leading to carcinoma formation. Understanding these mechanisms, alongside evaluating mucin characteristics and gene mutations, can deepen comprehension of GBC’s pathophysiology. This, in turn, facilitates the identification of high-risk individuals and the development of improved treatment strategies, ultimately enhancing patient outcomes. Thus, in this review, our aim has been to underscore the primary mechanisms underlying the development of gallbladder dysplasia and neoplasia.

Bladder cancer pathogenesis is closely linked to epigenetic alterations, particularly DNA methylation and demethylation processes. Environmental carcinogens and persistent inflammatory stimuli—such as recurrent urinary tract infections—can induce aberrant DNA methylation, altering gene expression profiles and contributing to malignant transformation. This review synthesizes current evidence on the role of DNA methyltransferases (DNMT1, DNMT3a, DNMT3b) and the hypermethylation of key tumour suppressor genes, including A2BP1, NPTX2, SOX11, PENK, NKX6-2, DBC1, MYO3A, and CA10, in bladder cancer. It also evaluates the therapeutic application of DNA-demethylating agents such as 5-azacytidine and highlights the impact of chronic inflammation on epigenetic regulation. Promoter hypermethylation of tumour suppressor genes leads to transcriptional silencing and unchecked cell proliferation. Urine-based DNA methylation assays provide a sensitive and specific method for non-invasive early detection, with single-target approaches offering high diagnostic precision. Animal models are increasingly employed to validate these findings, allowing the study of methylation dynamics and gene–environment interactions in vivo. DNA methylation represents a key epigenetic mechanism in bladder cancer, with significant diagnostic, prognostic, and therapeutic implications. Integration of human and experimental data supports the use of methylation-based biomarkers for early detection and targeted treatment, paving the way for personalized approaches in bladder cancer management.

Kidney injury molecule-1 (KIM-1) is a transmembrane protein that is significantly upregulated in renal cells following injury. It has considerable potential as a biomarker for diagnosing and monitoring renal cell carcinoma (RCC). This review examines KIM-1 expression across multiple biological sources—including tissue, blood, and urine—and highlights its strong association with RCC risk. Clinical studies have shown that KIM-1 levels decline within weeks after nephrectomy, underscoring its utility in assessing therapeutic response. Additionally, urinary KIM-1 levels correlate with histopathological outcomes following cisplatin treatment, supporting its role as a non-invasive marker for treatment effectiveness. Despite these promising findings, several challenges remain. These include variability in assay performance and the modulatory effects of the tumour microenvironment on KIM-1 expression. Overcoming these technical limitations is crucial for integrating KIM-1 into clinical workflows. Furthermore, its potential role in guiding combination therapies—such as tyrosine kinase inhibitors (TKIs), immune checkpoint inhibitors (ICIs), and mTOR inhibitors—could enhance therapeutic precision while minimizing toxicity. Continued research is essential to validate these applications and facilitate the routine clinical use of KIM-1 in RCC management.

Background: Although rare, Fournier’s gangrene is a major urological emergency. We aimed to learn more about the pathogenesis of Fournier’s gangrene and assess the antibiotic resistance patterns in individuals with this disease. Methods: We retrospectively evaluated the patients diagnosed with and treated for Fournier’s gangrene in a Neamt county hospital and “CI Parhon” Clinical Hospital in Iasi, Romania between 1 January 2016 and 1 June 2022. Results: We included a total of 40 patients, all males; of these, 12.5% died. In our study, in the patients that died, the adverse prognostic factors were a higher body temperature (38.12 ± 0.68 vs. 38.94 ± 0.85 °C; p = 0.009), an elevated WBC (17.4 ± 5.46 vs. 25.23 ± 7.48; p = 0.003), obesity (14.28% vs. 60%; p = 0.04), and a significantly higher FGSI (4.17 ± 2.80 vs. 9.4 ± 3.2; p = 0.0002) as well as MAR index (0.37 ± 0.29 vs. 0.59 ± 0.24; p = 0.036). These patients were more likely to have liver affections than those in the group who survived, but the difference was not significant. The most frequently identified microorganism in the tissue secretions culture was E. coli (40%), followed by Klebsiella pneumoniae (30%) and Enterococcus (10%). The highest MAR index was encountered in Acinetobacter (1), in a patient that did not survive, followed by Pseudomonas (0.85) and Proteus (0.75). Conclusions: Fournier’s gangrene remains a fatal condition, a highly resistant causative microorganism that is not always correlated with a poor prognosis.

Background: This study highlighted the differences between the biochemical compositions of urinary stones from patients with type 1 diabetes versus those with type 2 diabetes. Materials and Methods: This study included patients diagnosed with kidney stones and diabetes who were referred to the Urological Clinic of the Dr. C. I. Parhon Hospital in Iasi from April 2017 to April 2024. We analyzed the spectroscopic stone composition from 128 lithiasis patients treated in our Clinic. In the current study, the distribution of the biochemical composition of stones varied significantly between diabetic patients with type 2 diabetes, who formed primarily mixed uric acid stones, and diabetic patients with type 1 diabetes, who mainly developed pure uric acid stones (p < 0.001). Patients with uric acid stones had significantly higher mean creatinine values than the other stone types (p < 0.001). Urinary pH levels were abnormal for all biochemical subtypes of stones, indicating acidic urine. However, patients with uric acid stones had lower pH values than the group average. From the Kaplan–Mayer analysis, patients with pure uric acid stones had a shorter time to stone recurrence compared to patients with other biochemical types identified. Conclusions: These findings, which highlight the prevalence of pure uric acid stones in patients with type 1 diabetes and the impact of this on the strategy for dissolving pure stones, represent a significant advancement in understanding urinary lithiasis in diabetic patients.